title: Restrictive left ventricular filling patterns are predictive of diastolic ventricular interaction in chronic heart failure.
abstract: OBJECTIVE
  The purpose of this study was to determine whether restrictive left ventricular (LV) filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure.
  
  
  BACKGROUND
  We recently demonstrated a diastolic ventricular interaction in approximately 50% of a series of patients with chronic heart failure, as evidenced by paradoxic increases in LV end-diastolic volume despite reductions in right ventricular end-diastolic volume during volume unloading achieved by lower body negative pressure (LBNP). We reasoned that such an interaction would impede LV filling in mid and late diastole, but would be minimal in early diastole, resulting in a restrictive LV filling pattern.
  
  
  METHODS
  Transmitral flow was assessed using pulsed wave Doppler echocardiography in 30 patients with chronic heart failure and an LV ejection fraction < or = 35%. Peak early (E) and atrial (A) filling velocities and E wave deceleration time were measured. Left ventricular end-diastolic volume was measured using radionuclide ventriculography before and during -30-mm Hg LBNP.
  
  
  RESULTS
  Nine of the 11 patients with and 2 of the 16 patients without restrictive LV filling patterns (E/A > 2 or E/A 1 to 2 and E wave deceleration time < or = 140 ms) increased LV end-diastolic volume during LBNP (p = 0.001). The change in LV end-diastolic volume during LBNP was correlated with the baseline A wave velocity (r = -0.52, p = 0.005) and E/A ratio (r = 0.50, p = 0.01).
  
  
  CONCLUSIONS
  Restrictive LV filling patterns are associated with diastolic ventricular interaction in patients with chronic heart failure. Volume unloading in the setting of diastolic ventricular interaction allows for increased LV filling. Identifying patients with chronic heart failure and restrictive filling patterns may therefore indicate a group likely to benefit from additional vasodilator therapy.
authors.affiliation: Department of Cardiology, University of Wales College of Medicine, Cardiff, United Kingdom.
authors.forename: J J
authors.initials: JJ
authors.lastname: Atherton
authors.forename: T D
authors.initials: TD
authors.lastname: Moore
authors.forename: H L
authors.initials: HL
authors.lastname: Thomson
authors.forename: M P
authors.initials: MP
authors.lastname: Frenneaux
mesh_terms: D016279:Atrial Function, Left / Q000502:physiology; D016280:Atrial Function, Right / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology*; D002306:Cardiac Volume / Q000502:physiology; D003971:Diastole; D018619:Echocardiography, Doppler, Pulsed; D005260:Female; D005544:Forecasting; D015637:Gated Blood-Pool Imaging; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008150:Lower Body Negative Pressure; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000503:physiopathology; D019275:Radiopharmaceuticals; D013670:Sodium Pertechnetate Tc 99m; D013318:Stroke Volume / Q000502:physiology; D014665:Vasodilator Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D016278:Ventricular Function, Right / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D019275:Radiopharmaceuticals; D014665:Vasodilator Agents; D013670:Sodium Pertechnetate Tc 99m